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In the last 200 years, tuberculosis (TB) has been responsible for the deaths of over 1 billion people [Gagneux18]. More recently, after briefly falling behind COVID-19, TB has regained its title as the world's deadliest infectious disease [Ilic23, Orgeur24]. According to the World Health Organisation, in 2022, 10.6 million people around the world fell ill with this potentially deadly respiratory disease, and 1.3 million lost their lives [Orgeur24]. Originally named "tubercle bacillus" by German physician and microbiologist Robert Koch upon isolation in 1882, the etiological agent of TB is the actinobacterium Mycobacterium tuberculosis [Sakula83].
Mycobacterium tuberculosis is part of the Mycobacterium tuberculosis complex (MTBC), a group of highly related mycobacteria (>99% nucleotide sequence identity) with lineages adapted to causing disease in both humans and also wild and domestic animals [Gagneux18]. M. tuberculosis is characterized by qualities such as its persistence within alveolar macrophages, slow growth, ability to enter dormancy, complex cell envelope and evasion of host immunity [McDonough93, Cole98, Meena10, Rahlwes23, Bo23]. Unfortunately, this pathogen has also exhibited both multidrug resistance (MDR-TB) and extensive drug resistance (XDR-TB) [Gagneux18, Rahlwes23].
The genome represented by this PGDB belongs to Mycobacterium tuberculosis H37Rv. This strain and its avirulent counterpart, Mycobacterium tuberculosis H37Ra, are derivatives of M. tuberculosis H37, which was first isolated from the sputum of a 19 year old patient with chronic pulmonary tuberculosis at Saranac laboratory in 1905 [Steenken34, Santoro17]. The genome of M. tuberculosis H37Rv was first sequenced in 1998, and has since become the reference genome for members of the MTBC, undergoing subsequent re-annotation and resequencing to improve mycobacterial research efforts [Cole98, Camus02, Chitale22]. This PGDB has been extensively updated via manual curation. In addition, we have incorporated large datasets into the database characterizing the transcriptional regulatory network [Rustad14, Turkarslan15, Minch15], transcription start sites [Cortes13, Shell15], small RNAs [Stiens23, Miotto12], gene essentiality [DeJesus17], as well as information on anti-tuberculosis compounds.
We thank Professor Dirk Schnappinger (Weill Cornell Medical College) and Professor Thomas R. Ioerger (Texas A&M University) for their assistance in identifying recent advancements in M. tuberculosis research and relevant data collections for this PGDB.